ECG criteria
- Rhythm and heart rate: sinus tachycardia (the most frequent finding, non-specific)
- SI-QIII-TIII: S wave in lead I and Q wave with a negative T wave in lead III; the absence of a similar Q wave in lead II can be noted as a tentative, but not diagnostic, feature
- Rightward axis deviation or a sudden transition from normal to right-axis deviation compared with previous ECGs
- New incomplete right bundle branch block — QRS approximately 110–119 ms with rsR'/rSR' morphology in V1–V2; complete block — QRS ≥ 120 ms with the same morphology; new onset compared with a prior ECG increases the significance of the finding, but does not confirm PE on its own
- T-wave inversion in V1–V4 (a sign of right ventricular strain), sometimes also in leads III and aVF
- Rarely — ST-segment and J-point elevation in V1, aVR, and other leads in severe acute right ventricular strain (non-specific, requires exclusion of ACS)
- Rarely — P pulmonale (tall, peaked P wave ≥ 2.5 mm in lead II) as a non-specific sign of right atrial strain
- Inconsistent associated findings: low QRS voltage, new supraventricular arrhythmias (including atrial fibrillation) — carry no independent diagnostic value
What it looks like on ECG
The most common finding in PE is ordinary sinus tachycardia without other changes, therefore a normal or minimally altered ECG does not rule out the diagnosis. The classic but uncommon syndrome (occurring in less than a third of patients) SI-QIII-TIII consists of three components: a deep S wave in lead I, and a Q wave along with a negative T wave in lead III. This pattern is non-specific and optional: its presence or absence, including the distribution of the Q wave across leads II and III, cannot independently differentiate PE from an inferior myocardial infarction — clinical presentation, serial ECGs, troponin, and imaging are required for this.
In acute right ventricular strain, the electrical axis deviates to the right, and a new right bundle branch block may appear: incomplete — QRS of about 110–119 ms, complete — QRS ≥ 120 ms, both featuring typical rsR'/rSR' morphology in leads V1–V2 and corresponding changes in lateral leads. T-wave inversion is frequently visible in chest leads V1–V4, serving as a sign of right ventricular strain. In severe acute right ventricular strain, ST-T changes in V1–V4, aVR, and other leads (ST-segment and J-point elevation) are occasionally observed, but this pattern is not standardized, is non-specific, and requires ruling out ACS based on clinical presentation, serial ECGs, troponin, and imaging.
| Sign | Leads | What to look for |
|---|---|---|
| Tachycardia | all | Heart rate > 100 bpm |
| SI-QIII-TIII | I, III | S in I + Q and (–)T in III |
| RBBB (new) | V1–V2 | QRS 110–119 ms (incomplete) or ≥ 120 ms (complete) |
| T-wave inversion | V1–V4 | symmetric negative T |
| P pulmonale (rare) | II | P ≥ 2.5 mm |
All signs are evaluated in comparison with the patient's baseline (prior) ECG, if available — serial comparison is precisely what increases diagnostic value.
Mechanism
Acute mechanical obstruction of the pulmonary arteries by a thrombus sharply increases pulmonary vascular resistance. The right ventricle, unaccustomed to such a load, acutely dilates and suffers pressure overload. This shifts the electrical axis of the heart to the right, slows conduction down the right bundle branch due to myocardial stretch, and leads to subendocardial ischemia of the right ventricle, which manifests as T-wave inversion in the right precordial leads. Reflex and hypoxic activation of the sympathetic nervous system accounts for sinus tachycardia — the most consistent, albeit non-specific, sign.
Causes
- Thromboembolism from lower extremity and pelvic veins (most frequent source)
- Deep vein thrombosis of the upper extremities (catheter-associated)
- Fat, air, or amniotic fluid embolism (rare, different mechanism)
- Risk factors: immobilization, surgical procedures, oncology, pregnancy and the postpartum period, estrogen use, thrombophilia, prior venous thromboembolism
Differential diagnosis
- Inferior myocardial infarction: the distribution of the Q wave across leads II and III is variable in both conditions and does not differentiate them on its own; clinical presentation, serial ECGs, troponin, and imaging are decisive
- Anterior STEMI / ST elevation in aVR in multivessel disease: ST-T changes in V1 and aVR are possible in severe PE, but lack a consistent standard pattern; differentiation requires clinical correlation, troponin, and imaging
- COPD and chronic cor pulmonale: similar signs of right heart strain, but developing gradually rather than acutely; there is a history of chronic lung disease
- Normal variant of SI-QIII-TIII in healthy individuals: occurs without clinical symptoms of PE, particularly with a horizontal electrical axis; evaluated only in the context of symptoms
- Pericarditis: in the acute phase — diffuse (not restricted to the territory of a single coronary artery) concave ST elevation and PR segment depression; the typical T-wave inversion in V1–V4 seen in PE is atypical for acute-phase pericarditis, but may appear later in the evolutionary phase after ST normalization — therefore, differentiation relies on clinical presentation, serial ECGs, troponin, and imaging rather than a single tracing.
Clinical significance and management
The ECG is not used to confirm or rule out PE — its specificity and sensitivity are low, and approximately 10–25% of patients with confirmed PE may have a normal ECG (the exact proportion depends on severity and the studied cohort). The clinician's task is to notice signs of acute right ventricular strain (SI-QIII-TIII, T-wave inversion in V1–V4, new right bundle branch block) as an indication for urgent targeted workup. Management depends on the clinical probability of PE (Wells or Geneva scores): in low or intermediate probability, D-dimer is measured (with age-adjusted cutoffs for individuals over 50), and if positive, CT pulmonary angiography is performed; in high clinical probability, imaging is pursued immediately without waiting for D-dimer results. In shock, hemodynamic instability, or cardiac arrest, bedside echocardiography and emergency treatment algorithms take precedence; the ECG must not delay these interventions. The presence of ECG signs of right ventricular strain is associated with a more severe course and worse prognosis, which is why they are documented in the report and factored into risk stratification alongside echocardiography and biomarkers (troponin, NT-proBNP).
Common interpretation errors
- Searching only for SI-QIII-TIII and ruling out PE in its absence — the syndrome is present in less than a third of patients
- Relying on the distribution of the Q wave in leads II and III as a rule to distinguish PE from inferior MI without considering the clinical picture and serial changes
- Failing to compare with a prior ECG — it is precisely the new onset of bundle branch block or T-wave inversion that increases the value of the finding
- Interpreting ST elevation in V1/aVR in severe PE as an independent diagnostic criterion without assessing the clinical presentation and troponin levels
- Ignoring isolated sinus tachycardia as an "unimportant" finding when PE is suspected
SI-QIII-TIII — deep S in I, Q and negative T in III (not always present, easily remembered by lead letters)
1. Which ECG finding is most frequently observed in acute PE?
Sinus tachycardia is the most common, albeit non-specific, finding; the classic SI-QIII-TIII is less frequent.
2. Can the distribution of the Q wave in leads II and III reliably differentiate PE from an inferior myocardial infarction?
The distribution of the Q wave across leads is variable in both conditions and does not allow differentiation between PE and inferior MI on its own.
3. What is the role of the ECG in the diagnosis of PE?
The ECG has low sensitivity and specificity in PE; its value lies in detecting signs of right ventricular strain important for risk stratification.
Frequently asked questions
Can PE be ruled out by a normal ECG?
No. A normal ECG occurs in approximately 10–25% of patients with confirmed PE. Diagnosis is based on clinical probability, D-dimer, and imaging (CT pulmonary angiography) rather than the ECG.
Which is more common in PE — the SI-QIII-TIII pattern or tachycardia?
Sinus tachycardia is significantly more common, but it is completely nonspecific. SI-QIII-TIII is more characteristic, but is present in less than a third of patients.
How to differentiate PE from an inferior infarction by the Q wave in III?
There is no reliable ECG rule for Q wave distribution: PE can feature a small or transient Q in III, sometimes with T inversion, but its presence or absence in lead II is not a diagnostic criterion. PE and inferior MI must be differentiated based on clinical presentation, serial ECGs, troponin, and imaging.
Are ECG signs of right ventricular strain dangerous in PE?
Yes, their presence indicates a more pronounced hemodynamic load on the right ventricle and is associated with a worse prognosis, which strengthens the indications for urgent further examination and risk stratification.
Which ECG sign of PE is most common?
Sinus tachycardia is the most frequent, albeit nonspecific, finding. It is followed in frequency by T wave inversion in the right precordial leads and incomplete right bundle branch block.
ECG Course
Interpretation from basics to myocardial infarction — learn to read any ECG using a systematic algorithm.
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Related terms
More in the section "Pericardium, Lungs, Brain and Others"
Sources
- Goldberger A.L. et al. Clinical Electrocardiography: A Simplified Approach
- Surawicz B., Knilans T.K. Chou's Electrocardiography in Clinical Practice
- Hampton J.R. The ECG in Practice
- Clinical guidelines of the Russian Ministry of Health on pulmonary embolism
Educational material for medical students and physicians. Does not replace clinical guidelines and physical examination; the ECG must always be interpreted in conjunction with the clinical picture.